Gilmour K M, Desforges P R, Perry S F
Department of Biology, Carleton University, 1125 Colonel By Drive, Ottawa, Ont., Canada K1S 5B6.
Respir Physiol Neurobiol. 2004 May 20;140(2):173-87. doi: 10.1016/j.resp.2004.02.001.
Theory suggests that HCO3- dehydration in the plasma of rainbow trout is limited by both the absence of carbonic anhydrase (CA) activity and the low non-bicarbonate buffer capacity of the plasma (betaplasma). The potential for betaplasma to limit plasma HCO3- dehydration was assessed in rainbow trout in which HCO3- dehydration via the red blood cell (RBC) was inhibited using the anion exchange blocker 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS). DIDS administration reduced the rate of RBC HCO3- dehydration by 68-80% for at least 6h, resulting in the elevation of arterial CO2 tension (PaCO2) by 3.07 +/- 0.45 Torr (N = 6). Addition of bovine CA to the circulation of DIDS-treated trout caused PaCO2 to decrease significantly. This effect was increased significantly in rainbow trout in which betaplasma was elevated experimentally by intravascular injection of N-[2-hydroxyethyl]piperazine-N'-[2-ethanesulfonic acid] (HEPES), supporting the hypothesis that CA-catalysed HCO3- dehydration in the plasma of rainbow trout is limited by proton availability.
理论表明，虹鳟鱼血浆中HCO₃⁻脱水受到两种因素限制，一是缺乏碳酸酐酶（CA）活性，二是血浆（β血浆）的非碳酸氢盐缓冲能力较低。在虹鳟鱼中评估了β血浆限制血浆HCO₃⁻脱水的可能性，在这些虹鳟鱼中，使用阴离子交换阻滞剂4,4'-二异硫氰基芪-2,2'-二磺酸（DIDS）抑制通过红细胞（RBC）的HCO₃⁻脱水。给予DIDS至少6小时内使RBC的HCO₃⁻脱水速率降低了68 - 80%，导致动脉血二氧化碳分压（PaCO₂）升高3.07±0.45托（N = 6）。向经DIDS处理的虹鳟鱼循环系统中添加牛CA可使PaCO₂显著降低。在通过血管内注射N-[2-羟乙基]哌嗪-N'-[2-乙磺酸]（HEPES）实验性升高β血浆的虹鳟鱼中，这种效应显著增强，支持了虹鳟鱼血浆中CA催化的HCO₃⁻脱水受质子可用性限制的假说。
